Extra Oxygen Consumption Research Articles

Acute cardiovascular responses to unilateral bicep curls with blood flow restriction

Background/ObjectivesA consensus on the acute cardiovascular responses to low intensity (LI) resistance exercise (RE) combined with blood flow restriction (BFR) has not yet been reached. This study was designed to compare acute cardiovascular responses to a single bout of LIRE, high intensity (HI) RE, and LIRE with BFR in physically active young males. MethodsParticipants completed 3 RE sessions in random order, where each session consists of 4 sets of unilateral dumbbell bicep curls. Cardiovascular hemodynamics were measured at baseline and right after each set of RE. ResultsAortic augmentation index (AIx) was significantly higher after set 2,3,4 of RE in LI + BFR session compared to LI session (P < 0.05). Brachial systolic blood pressure (SBP), heart rate (HR), brachial rate pressure product (RPP), and central RPP responses did not differ between LI and LI + BFR sessions (P > 0.05). HI session had a higher central SBP, brachial RPP, central RPP, and aortic AIx compared to LI session after each set of RE (P < 0.05), but not brachial SBP (P > 0.05). ConclusionsTaken together, this study showed that LIRE combined with BFR acutely augmented aortic stiffness, as also observed in HI session, but myocardial oxygen consumption was only higher in HI session when compared to LI session. Thus, although BFR did not exaggerate cardiovascular responses nor cause extra myocardial oxygen consumption, it should be prescribed with caution when control of acute aortic stiffening is necessary during RE.

Effects of ranolazine on fatty acid transformation in the isolated perfused rat liver

It has been proposed that in the heart, ranolazine shifts the energy source from fatty acids to glucose oxidation by inhibiting fatty acid oxidation. Up to now no mechanism for this inhibition has been proposed. The purpose of this study was to investigate if ranolazine also affects hepatic fatty acid oxidation, with especial emphasis on cell membrane permeation based on the observations that the compound interacts with biological membranes. The isolated perfused rat liver was used, and [1-(14)C]oleate transport was measured by means of the multiple-indicator dilution technique. Ranolazine inhibited net uptake of [1-(14)C]-oleate by impairing transport of this fatty acid. The compound also diminished the extra oxygen consumption and ketogenesis driven by oleate and the mitochondrial NADH/NAD(+) ratio, but stimulated (14)CO(2) production. These effects were already significant at 20μM ranolazine. Ranolazine also inhibited both oxygen consumption and ketogenesis driven by endogenous fatty acids in substrate-free perfused livers. In isolated mitochondria ranolazine inhibited acyl-CoA oxidation and β-hydroxybutyrate or α-ketoglutarate oxidation coupled to ADP phosphorylation. It was concluded that ranolazine inhibits fatty acid uptake and oxidation in the liver by at least two mechanisms: inhibition of cell membrane permeation and by an inhibition of the mitochondrial electron transfer via pyridine nucleotides.

Zonation of alanine metabolism in the bivascularly perfused rat liver

Zonation of alanine metabolism was investigated in the bivascularly perfused rat liver, a technique in which a selective area of the periportal region can be reached via the hepatic artery. Bivascular liver perfusion was done in both the antegrade and retrograde modes. Predominance of a given metabolic parameter in the periportal or perivenous area was deduced from comparisons of the changes caused by alanine infusion into the hepatic artery in antegrade and retrograde perfusion. Confirming previous notions, glutamine synthesis predominated in the perivenous area, however, the contribution of the periportal area was significant. Gluconeogenesis and the associated extra oxygen consumption were more pronounced in the periportal region. The capacity of urea synthesis in the periportal region was relatively small as indicated by the ratios of urea to glucose production, which were lower in this region. Ammonia in the periportal region was considerably above the mean ammonia production of whole the liver parenchyma. The overflows of pyruvate and lactate were considerably smaller in the periportal region. The distribution of alanine metabolism seems to reflect mainly zonation of the fates of the carbon skeleton (mainly gluconeogenesis). The production of glutamine in the periportal area is in agreement with recent reports about the presence of glutamine synthetase in Kupffer and endothelial cells.

Endogenous respiration reflects the energy load imposed by transport of nonmetabolizable substrates and by induced de novo protein synthesis in Rhodotorula glutinis

Uptake of the nonmetabolizable sugars 6-deoxy-d-glucose, l-rhamnose and l-xylose, which are taken up by a common carrier, stimulated significantly cell respiration in Rhodotorula glutinis. The extra oxygen consumption for uptake (0.5–0.7 equivalents O2/mol transported sugar) was proportional to the uptake rate and was independent of the Ktvalue of the transport system. Sugars that become metabolized after induction, d-arabinose and methyl-α-d-glucoside, caused a higher stimulation, 1.4 and 3.6 equivalents O2/mol respectively, which was reduced to 0.6 equivalents O2/mol when de novo protein synthesis was blocked by cycloheximide. The stimulation of respiration thus includes a fraction related purely to the energy demand for uptake and another one related to the induced de novo protein synthesis. The net uptake-induced respiration boost was similar with all sugars under study irrespective of their transport systems. The estimated energy demand was equivalent to about 2 ATP/sugar molecule. For comparison, the amino acid analogue α-aminoisobutyric acid (AIB) was also investigated; the overall energy demand for its uptake corresponded to the equivalent of about 4 ATP/molecule.

Limitations to V̇ O 2max in humans after blood retransfusion

Seven young, healthy male subjects performed maximal exercise on a cycloergometer with central venous and arterial catheters, before and after autologous retransfusion of red blood cells. Maximal oxygen consumption (V̇ O 2max ), blood gas composition and haemodynamic variables were measured, in order to test the hypothesis of monofactorial vs polyfactorial V̇ O 2max limitation. Autologous blood retransfusion led to significant increases in haemoglobin concentration and consequently arterial oxygen concentration during maximal exercise, while maximal cardiac output, heart rate and stroke volume were not significantly changed. The relationship between maximal oxygen delivery (cardiac output·arterial oxygen concentration; (Q̇·Ca O 2 ) max and maximal oxygen consumption in this study was V̇ O 2max (L·min −1) = 0.02 +0.64·(Q̇·Ca O 2 ) max (L·min −1), the slope being significantly less than unity. These results suggest that (Q̇·Ca O 2 ) max plays but a fractional role in limiting V̇ O 2max , in agreement with recent models concerning the resistance to oxygen flow in the respiratory system (di Prampero and Ferretti, Respir. Physiol. 80: 113–128, 1990). The relative increase in V̇ O 2max after blood retransfusion matched the relative increase in ‘aerobic performance’, measured as the maximal power output that could be maintained aerobically for 30 min. Furthermore, the increase in maximal power output (15 ± 3 watts) could account for almost all of the extra oxygen consumption. This match suggests that there is an inability to fully utilize muscle oxidative capacity in the normocythaemic state.

The contribution of ATP turnover by the Na +/K +-ATPase to the rate of respiration of hepatocytes : Effects of thyroid status and fatty acids

In less than 1 min ouabain maximally inhibits oxygen consumption due to gramicidin-induced ATP turnover by the Na+/K+-ATPase in hepatocytes. Ouabain rapidly inhibits respiration on palmitate or glucose by only 6-10% indicating that the Na+/K+-ATPase plays a minor role in cell ATP turnover. 29% of the extra oxygen consumption of hepatocytes isolated from hyperthyroid rats was inhibited by ouabain showing that the Na+/K+-ATPase is responsible for some but not the majority of the stimulation of respiration induced by thyroid hormone.

The response to monochromatic light flashes of the oxygen consumption of honeybee drone photoreceptors.

Local measurements of the fall in oxygen pressure on stimulation of slices of the retina of the honeybee drone by flashes of light were made with oxygen microelectrodes and used to calculate the kinetics of the extra oxygen consumption (delta QO2) induced by each flash. The action spectrum for delta QO2 was obtained from response-intensity curves in response to brief (40 ms) monochromatic light flashes. The action spectrum of receptor potentials was obtained with the same experimental conditions. The two action spectra match closely: they deviate slightly from the photosensitivity spectrum of the drone rhodopsin (R). The deviation is thought to be due to wavelength-dependent light scattering and absorption in the preparation. In these experiments, the visual pigment was first illuminated with orange light, which is known to convert the bistable drone photopigment predominantly to the R state from the metarhodopsin (M) state. When long (300-900 ms) light flashes were used to elicit delta QO2, the responses to different wavelengths could not be matched in time course (as for the short flashes). Flashes producing large R-to-M conversions produced a prolonged delta QO2. The prolongation did not occur after double flashes, which produced both large R-to-M and M-to-R conversions. Similar changes in the length of afterpotentials in the photoreceptor cells and in a long-lasting decrease in photoreceptor intracellular K+ activity were found after long single or double flashes. The results are interpreted to show that the initial event for stimulation by light of metabolism in the drone retina is the same as that for stimulation of electrical responses (i.e., absorption of photons by R). Absorption of photons by M can produce an inhibitory effect on this stimulation.

The oxidation of extracellular NADH by sugarcane cells: Coupling to ferricyanide reduction, oxygen uptake and pH change

Suspension-cultured cells of sugarcane (Saccharum sp. hybrids) did not oxidize exogenously supplied NADH in the absence of ferricyanide (potassium hexacyanoferrate [III]), whereas they did at a low rate in the presence of ferricyanide. Concomitantly, ferricyanide was reduced at a slow rate. Neither a pH change nor a change in respiration was caused by the addition of NADH and-or ferricyanide, but ferricyanide was a strong inhibitor of sugar transport. In contrast to cells, protoplasts rapidly oxidized exogenous NADH. This oxidation was accompanied by an increase in oxygen consumption and a net proton disappearance from the medium. Exogenous ferricyanide was reduced only slowly by protoplasts. Simultaneous presence of NADH and ferricyanide produced two effects: 1) a very rapid stoichiometric oxidation of NADH and reduction of ferricyanide until one of the reaction compounds was exhausted, and 2) a nearly instantaneous inhibition of the slower phase of NADH oxidation, which was observed in the presence of NADH but absence of ferricyanide. The extra oxygen consumption and the alkalinization of the medium, as observed with NADH, were also immediately stopped by ferric ions and ferrous ions. The presence of NADH and ferricyanide caused a fast stoichiometric acidification of the medium. These results were taken as evidence that the oxidation of NADH in the absence of ferricyanide is not related to the NADH-ferricyanide-coupled redox reaction. Furthermore, addition of NADH caused some uncoupling of the protoplasts, an effect which would explain the strong acidification of the cell cytoplasm and the inhibition of various transport systems. The NADH-oxidizing systems oxidized both the β-configurated pyridine nucleotide and the α-configurated form. Since NADH-linked dehydrogenases usually do not work with α-NADH (with the exception of the endoplasmic-reticulum-bound electron-transport system), the observed activities could have been derived from contaminating membranes and dying protoplasts in the suspension. All reported reactions partly or predominantly occurred in the supernatant of the protoplast suspension and increased considerably during incubation of the protoplasts. The rates and quantities of oxygen consumption, pH change, and ferricyanide reduction fitted with NADH oxidation in a stoichiometric ratio, which implied that all these reactions occurred in the extracellular space, without involving transmembrane steps. No evidence for a physiological role in energization of the plasmalemma was found.

The Recovery From a Transient Inhibition of the Oxidative Metabolism of the Photoreceptors of the Drone (Apis Mellifera ♂)

ABSTRACT In the honey-bee drone retina (Apis mellifera) oxidative metabolism is carried out largely by the photoreceptors. We have studied the effects of a transient inhibition of this metabolism, by recording receptor potential simultaneously with measurements of local and extracellular [K+] ([K+]o), using O2-and K+-sensitive microelectrodes. When the retina was subjected to anoxia or exposed to Na-amobarbital (amytal), the photoreceptors depolarized by about 30 my, in parallel with an increase of [K+]o of up to 30 mmol 1−1, and the receptor potential was abolished in 2–3 min. The reduction of the receptor potential followed the beginning of anoxia with a delay, which we define as a ‘resistance’ of the photoreceptors to anoxia. The resistance to anoxia was greater if the photoreceptors were stimulated with only low intensity light flashes, suggesting that the effects of anoxia are due to the progressive consumption of a substance stored in the photoreceptors. This substance is probably ATP. When O2 was reintroduced, or amytal washed out, oxidative metabolism rapidly resumed. [K+]o quickly decreased and, after a large undershoot, returned to the baseline in less than 5 min. There was in parallel a repolarization of the photoreceptors, followed by recovery of the receptor potential. About 5 min after réintroduction of O2, when the [K+]o, the membrane potential and the amplitude and kinetics of the receptor potential had completely recovered, exposure of the retina to a second anoxia suppressed the receptor potential faster than had the first anoxia. Full recovery of the resistance to anoxia thus takes longer (by about 10 min) than recovery of the electrical properties of the photoreceptor cells. The amplitude of the extra oxygen consumption measured after a flash of light recovered in parallel with the resistance to anoxia.

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

Oxygen uptake occurs faster than sodium pumping in bee retina after a light flash.

When neurones are active there is an entry of Na+, which must subsequently be pumped out, and an increase in their oxygen consumption rate (Qo2). The Na+ pump derives its energy from ATP, splitting it into ADP and Pi, and it has reasonably been proposed that the changes in concentrations of ATP, ADP and Pi lead to a stimulation of the O2 consumption by the mitochondria and hence to a restoration of the stock of ATP. Here we present evidence suggesting that Qo2 must be controlled differently in the retinal photoreceptor cells of the honeybee drone. Stimulation of drone photoreceptors with a flash of light causes an entry of Na+ (ref. 4) and a transient increase in Qo2 that indicates respiration of the right order of magnitude to provide ATP to pump the Na+ out. We report intracellular recordings of changes in intracellular sodium (Nai+) and potassium (Ki+) in response to single light flashes and have compared the time course of extra oxygen consumption (delta Qo2) with these ion changes and other indices of Na+ pumping. We found that the time course of pumping seems to lag behind the time course of delta Qo2. It follows that the mitochondrial respiration must be stimulated by some signal which is generated earlier than the rise in ADP produced by the Na+ pump.

Phosphate efflux and oxygen consumption in small non‐myelinated nerve fibres at rest and during activity

1. The oxygen consumption and the movements of labelled phosphate were measured in garfish olfactory nerve at rest and during activity.2. In solutions with 2.5 mM-K and 0.2 mM-phosphate the resting oxygen consumption was 0.206 m-mole/kg.min; activity at 2 sec(-1) produced an extra oxygen consumption of 2.46 mumole/kg.impulse. The extra oxygen consumption declined exponentially with a time constant of 2.62 min at 22-26 degrees C.3. The phosphate efflux, measured simultaneously, had a resting efflux rate constant of 1.24 x 10(-3) min(-1); activity at 2 sec(-1) produced an extra fractional loss of 9.38 x 10(-6) impulse(-1). The increase in phosphate efflux followed almost the same time course as the increase in oxygen consumption.4. Increasing the frequency of stimulation from 2 sec(-1) to 3 or 5 sec(-1) decreased both the extra oxygen consumption and the extra fractional loss of phosphate. When the frequency was decreased to 0.5 or 1 sec(-1) the extra oxygen consumption per impulse increased, while the extra phosphate liberation was lowered.5. Changing the phosphate concentration did not much affect the extra oxygen consumption; on the other hand, lowering or increasing the phosphate from the standard 0.2 mM decreased both the resting and the stimulated phosphate efflux.6. Lowering the K from the standard 2.5 mM did not affect the extra oxygen consumption, but increased both the resting and the extra loss of phosphate. At higher K concentrations the extra oxygen consumption and the extra fractional loss of phosphate decreased without much change in the resting phosphate efflux.7. Application of 1-20 muM-strophanthidin produced a transient decrease in the resting phosphate efflux without much change in resting oxygen consumption. With 10 or 20 muM-strophanthidin the extra fractional loss of phosphate and the extra oxygen consumption were both lowered in approximately the same proportions.8. The findings are consistent with the hypothesis that the increase in intracellular inorganic phosphate that results from increased break-down of ATP after activity, is the main cause for the increased phosphate efflux. A fraction of the increase in intracellular phosphate only appears to be liberated to the outside, the value of the fraction depending on the resting phosphate efflux before activity.9. The initial increase in intracellular inorganic phosphate after an impulse, estimated from the oxygen consumption or the phosphate fluxes, appears to be about 12-19 mumole/kg nerve, remarkably close to the value known from chemical analysis.

Quantitative analysis of the front crawl in men and women.

Body drag, D, and the overall mechanical efficiency of swimming, e, were measured from the relationship between extra oxygen consumption and extra drag loads in 42 male and 22 female competitive swimmers using the front crawl at speeds ranging from 0.4 to 1.2 m/s. D increased from 3.4 (1.9) kg at 0.5 m/s to 8.2 (7.0) kg at 1.2 m/s, with D of women (in brackets) being significantly less (P less than 0.05) than that of men. Mechanical efficiency increased from 2.9% at 0.5 m/s to 7.4% at 1.2 m/s for men, the values for women being somewhat greater than those for men. The ratio, D/e was shown to be identical to the directly measured energy cost of swimming one unit distance, V02/d, and was independent of the velocity up to 1.2 m/s. It averaged 52 and 37 l/km for men and women respectively (P less than 0.05). When corrected for body surface area the values were 27 and 22 l/km-m2 for men and women, respectively (P less than 0.05). The underwater torque, T, a measure of the tendency of the feet to sink, was 1.44 kg-m for men and 0.70 kg-m for women (P less than 0.05). VO2/d increased linearly with T for both men and women of similar competitive experience. However, the proportionality constant delta VO2/d-delta T was significantly less for competitive than noncompetitive swimmers. The analysis of the relationship VO2/d vs. T provides a valuable approach to the understanding of the energetics of swimming.

Sodium chloride stimulated respiration of Anacystis nidulans

AbstractWith certain salts a stimulation of respiration of the blue‐green alga Anacystis nidulans was found in the dark. The stimulation was observed only at high concentrations (10−2 M—10−1M). NaCl or LiCl are the most effective salts and on addition the increase of the respiration is about 2.5fold. Li is assumed to function as a substitute for Na. Potassium salts, except KCl, are ineffective. The order for the effectiveness is: NaCl &gt; NaNO3, Na2SO4 &gt; KCl &gt; KNO3, K2SO4 (=zero). Accordingly, the cation Na+, and to a less degree the anion Cl are responsible for the stimulatory effect. K, which is ineffective, is passively accumulated by Anacystis according to the membrane potential. Na is actively extruded. At 0.1 M external NaCl, the passive influx of Na is high, but even then it is balanced by an active efflux. This increases the energy consumption of the cells and leads to a stimulated respiration. With DCCD (N,N′‐dicyclohexylcarbodiimide) or NEM (N‐ethylmaleimide), the Na efflux is inhibited, simultaneously the stimulation of respiration is abolished and the passive influx of Na becomes detectable. At 0.1 M NaCl, the passive influx of Na measured in presence of DCCD is 5 × 10−6 moles Na/min and ml packed cells. In absence of DCCD on addition of 0.1 M NaCl the extra oxygen consumption is 2 × 10−6 moles O2/min and ml cells. This may prove that the stimulation of respiration is mainly caused by the active Na extrusion.

Sodium chloride stimulated respiration ofAnacystis nidulans

With certain salts a stimulation of respiration of the blue-green alga Anacystis nidulans was found in the dark. The stimulation was observed only at high concentrations (10(-2)M--10(-1)M). NaCl or LiCl are the most effective salts and on addition the increase of the respiration is about 2.5fold. Li is assumed to function as a substitute for Na. Potassium salts, except KCl, are ineffective. The order for the effectiveness is: NaCl greater than NaNO3, Na2SO4 greater than KCl greater than KNO3, K2SO4 (=zero). Accordingly, the cation Na+, and to a less degree the anion Cl- are responsible for the stimulatory effect. K, which is ineffective, is passively accumulated by Anacystis according to the membrane potential. Na is actively extruded. At 0.1 M external NaCl, the passive influx of Na is high, but even then it is balanced by an active efflux. This increases the energy consumption of the cells and leads to a stimulated respiration. With DCCD (N,N'-dicyclohexylcarbodiimide) or NEM (N-ethylmaleimide), the Na efflux is inhibited, simultaneously the stimulation of respiration is abolished and the passive influx of Na becomes detectable. At 0.1 M NaCl, the passive influx of Na measured in presence of DCCD is 5 x 10(-6) moles Na/min and ml packed cells. In absence of DCCD on addition of 0.1 M NaCl the extra oxygen consumption is 2 x 10(-6) moles O2/min and ml cells. This may prove that the stimulation of respiration is mainly caused by the active Na extrusion.

Further studies on the effect of phosphoenolpyruvate on respiration-dependent calcium transport by rat heart mitochondria

Phosphoenolpyruvate was found to depress extra oxygen consumption associated with Ca 2+-induced respiratory jump by rat heart mitochondria. Addition of phosphoenolpyruvate to mitochondria which have accumulated Ca 2+ in the presence of glutamate and inorganic phosphate causes the release of Ca 2+ from mitochondria. The phosphoenolpyruvate-stimulated Ca 2+ efflux can be observed with mitochondria loaded with low initial Ca 2+ concentration (0.12 mM) in the incubation medium. Measurements of mitochondrial H + translocation produced by addition of Ca 2+ to respiring mitochondria show that phosphoenolpyruvate depresses H + ejection and enhances H + uptake by mitochondria. The Ca 2+-releasing effect of phosphoenolpyruvate was found to be significantly stronger than that produced by rotenone when added to mitochondria loaded with Ca 2+ in the presence of glutamate and inorganic phosphate. Dithiothreitol cannot overcome the effect of phosphoenolpyruvate on mitochondrial Ca 2+ transport.

Effects of Octanoate and Oleate on Energy Metabolism in the Perfused Rat Liver

The effects of octanoate and oleate were studied in the isolated fasted rat liver perfused without substrate and were compared with the effects of lactate. Measurements were made of hepatic adenine nucleotide content, formation of ketone bodies, urea and glucose and uptake of fatty acids, lactate and oxygen. Calculations of the Krebs cycle activity and the flux through the oxidation at C‐3 were carried out. Comparing the extra oxygen consumption with extra ATP needs after addition of the fatty acids or lactate, ADP: O ratios were estimated for fatty acid oxidation and lactate gluconeogenesis.1. Octanoate as well as oleate induced a net decrease in ATP and an increase in AMP content of the liver. Total adenine nucleotides were unaltered. ATP:ADP ratios were lowered while the adenylate kinase mass‐action ratio increased.2. The Krebs cycle activity was suppressed by both fatty acids and enhanced by lactate. Oxidation at C‐3 was strongly stimulated by the fatty acids and was unaffected by lactate.3. An apparent ADP:O ratio of 2.7 was obtained after lactate addition, indicating a tightly coupled oxidative phosphorylation for the liver preparations used. Octanoate and oleate gave extremely low ratios of near one and near zero respectively.4. Perfusion with oligomycin caused a severe drop in oxygen uptake by the liver, which was unaltered after addition of fatty acids. Oligomycin added after the fatty acids caused an immediate fall in oxygen uptake to the level observed with oligomycin alone. 2,4‐Dinitrophenol was able to stimulate the oligomycin‐depressed respiration, both in the absence and in the presence of fatty acids. These results indicate that under our experimental conditions the fatty acids had no uncoupling effect and that microsomal fatty acid oxidation had to be minimal.5. Incorporation of [3H]leucine into proteins in liver and medium remained unchanged after addition of fatty acids, indicating that the low apparent ADP:O ratios are not the result of an enhanced synthesis of proteins.6. The possible relationship between fatty acid transport, energy‐wasting futile cycles and the low apparent ADP:O ratios observed during fatty acid oxidation is discussed.

Role of phosphate and other proton-donating anions in respiration-coupled transport of Ca2+ by mitochondria.

Measurements of extra oxygen consumption, (45)Ca(2+) uptake, and the osmotic expansion of the matrix compartment show that not all permeant anions are capable of supporting and accompanying the energy-dependent transport of Ca(2+) from the medium into the matrix in respiring rat-liver mitochondria. Phosphate, arsenate, acetate, butyrate, beta-hydroxybutyrate, lactate, and bicarbonate + CO(2) supported Ca(2+) uptake, whereas the permeant anions, nitrate, thiocyanate, chlorate, and perchlorate, did not. The active anions share a common denominator, the potential ability to donate a proton to the mitochondrial matrix; the inactive anions lack this capacity. Phosphate and the other active permeant anions move into the matrix in response to the alkaline-inside electrochemical gradient of protons generated across the mitochondrial membrane by electron transport, thus forming a negative-inside anion gradient. It is postulated that the latter gradient is the immediate "pulling" force for the influx of Ca(2+) on the electrogenic Ca(2+) carrier in respiring mitochondria under intracellular conditions. Since mitochondria in the cell are normally exposed to an excess of phosphate (and the bicarbonate-CO(2) system), particularly in state 4, inward transport of these proton-yielding anions probably precedes and is necessary for inward transport of Ca(2+) and other cations under biological conditions. These observations indicate that a negative-inside gradient of phosphate generated by electron transport is a common step and provides the immediate motive power not only for (a) the inward transport of dicarboxylates and tricarboxylates and (b) the energy-dependent exchange of external ADP(3-) for internal ATP(4-) during oxidative phosphorylation, as has already been established, but also for (c) the inward transport of Ca(2+), K(+), and other cations.

Energy expenditure of running kangaroo rats Dipodomys merriami

1. 1. The energetic cost of running on a motor driven treadmill was evaluated in kangaroo rats, Dipodomys merriami. 2. 2. Energy expenditure increases rectilinearly with increasing speed. 3. 3. The cost of running at 6°C is 17 per cent higher than its cost at 25 and 34°C. 4. 4. Under our conditions heat produced by exercise does not substitute for shivering at cold temperature. 5. 5. The greater portion of after-work extra oxygen consumption is recovered within 30 to 40 min. 6. 6. A description of a treadmill-metabolism apparatus for small animals is presented.

The effect of prolonged cold exposure on heat production in new-born rabbits.

1. The rates of oxygen consumption and the colonic temperatures were monitored from birth in rabbits delivered by Caesarean section at term. The rates of oxygen consumption at 25 and 36 degrees C rose over the first 12 hr of life.2. Thirty rabbits were kept unfed in an environment of 25 degrees C from birth. Extra oxygen consumption, in response to cold exposure, failed 24-34 hr later. Twenty-four of these rabbits were allowed to recover in an environment of 36 degrees C. The metabolic response to cold exposure did not return in those kept unfed or given glucose but those fed with rabbit's milk showed significant recovery when re-exposed to cold 4 or 18 hr later.3. The tissue glyceride content of brown and white adipose tissue and the liver were greatly reduced once the animals failed to respond to cold exposure and no significant rise was detected during the recovery period after a milk feed.4. Another twelve rabbits were kept unfed in an environment of 36 degrees C. These animals showed a poor metabolic response to cold exposure after 48 hr, although their brown adipose tissue was still replete with fat and the blood glucose rose to normal values during cold exposure.5. These results suggest that an increase in oxygen consumption in response to cold exposure can occur even though brown adipose tissue is largely depleted of glyceride provided that an alternative supply of fuel is available. Glucose alone is not an adequate source of energy.